• Michael Schwameis, Andreas Schober, Christian Schörgenhofer, Wolfgang Reinhard Sperr, Herbert Schöchl, Karin Janata-Schwatczek, Erol Istepan Kürkciyan, Fritz Sterz, and Bernd Jilma.
• 1Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria. 2Department of Emergency Medicine, Medical University of Vienna, Vienna, Austria. 3Division of Hematology and Hemostaseology, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria. 4Department of Anaesthesiology and Intensive Care Medicine, AUVA Trauma Centre Salzburg, Salzburg, Austria.
• Crit. Care Med. 2015 Nov 1;43(11):2394-402.

ObjectiveTo date, no study has systematically investigated the impact of drowning-induced asphyxia on hemostasis. Our objective was to test the hypothesis that asphyxia induces bleeding by hyperfibrinolytic disseminated intravascular coagulation.DesignObservational study.SettingA 2,100-bed tertiary care facility in Vienna, Austria, Europe.PatientsAll cases of drowning-induced asphyxia (n=49) were compared with other patients with cardiopulmonary resuscitation (n=116) and to patients with acute promyelocytic leukemia (n=83). Six drowning victims were investigated prospectively. To study the mechanism, a forearm-ischemia model was used in 20 volunteers to investigate whether hypoxia releases tissue plasminogen activator.InterventionsNone.Measurements And Main ResultsEighty percent of patients with drowning-induced asphyxia developed overt disseminated intravascular coagulation within 24 hours. When compared with nondrowning cardiac arrest patients, drowning patients had a 13 times higher prevalence of overt disseminated intravascular coagulation at admission (55% vs 4%; p<0.001). Despite comparable disseminated intravascular coagulation scores, acute promyelocytic leukemia patients had higher fibrinogen but lower d-dimer levels and platelet counts than drowning patients (p<0.001). Drowning victims had a three-fold longer activated partial thromboplastin time (124 s; p<0.001) than both nondrowning cardiac arrest and acute promyelocytic leukemia patients. Hyperfibrinolysis was reflected by up to 1,000-fold increased d-dimer levels, greater than 5-fold elevated plasmin antiplasmin levels, and a complete absence of thrombelastometric clotting patterns, which was reversed by antifibrinolytics and heparinase. Thirty minutes of forearm-ischemia increased tissue plasminogen activator 31-fold (p<0.001).ConclusionsThe vast majority of drowning patients develops overt hyperfibrinolytic disseminated intravascular coagulation, partly caused by hypoxia induced tissue plasminogen activator release. Antifibrinolytics and heparinase partially reverse the abnormal clotting patterns. Severe activated partial thromboplastin time prolongation may be a marker of combined hyperfibrinolytic afibrinogenemia and autoheparinization in drowning-related asphyxia.

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